Evidence map›Paper›PMID 27254784›Full record

ArticleAmerican journal of respiratory cell and molecular biology2016

Endothelial Monocyte-Activating Polypeptide II Mediates Macrophage Migration in the Development of Hyperoxia-Induced Lung Disease of Prematurity.

Daniel D Lee, Charitharth V Lal, Elizabeth A Persad, Chinn-Woan Lowe, Anna M Schwarz, Niranjan Awasthi, Roderich E Schwarz, Margaret A Schwarz

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 23 citations in OpenAlex.

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  7. Mechanistic regulation of SPHK1 expression and translocation by EMAP II in pulmonary smooth muscle cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Article
  8. Halogen exposure injury in the developing lung.Annals of the New York Academy of Sciences · 2020
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Daniel D Lee1 Departments of Pediatrics and.
Charitharth V Lal2 Department of Pediatrics, University of Alabama-Birmingham, Birmingham, Alabama.
Elizabeth A Persad3 Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas; and.
Chinn-Woan Lowe1 Departments of Pediatrics and.
Anna M Schwarz3 Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas; and.
Niranjan Awasthi4 Surgery, Indiana University, South Bend, Indiana.
Roderich E Schwarz4 Surgery, Indiana University, South Bend, Indiana.
Margaret A Schwarz1 Departments of Pediatrics and.
Indiana University South Bend · USThe University of Texas Southwestern Medical Center · USIndiana University Health · USUniversity of Alabama at Birmingham · USUniversity of Notre Dame · US

Funding

EMAP II: Pulmonary Vascular MediatorR01HL114977 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SCHWARZ, MARGARET A · 2012 to 2015
$1.8M
NHLBI NIH HHS R01 HL114977
6 · The paper itself

Abstract

Myeloid cells are key factors in the progression of bronchopulmonary dysplasia (BPD) pathogenesis. Endothelial monocyte-activating polypeptide II (EMAP II) mediates myeloid cell trafficking. The origin and physiological mechanism by which EMAP II affects pathogenesis in BPD is unknown. The objective was to determine the functional consequences of elevated EMAP II levels in the pathogenesis of murine BPD and to investigate EMAP II neutralization as a therapeutic strategy. Three neonatal mouse models were used: (1) BPD (hyperoxia), (2) EMAP II delivery, and (3) BPD with neutralizing EMAP II antibody treatments. Chemokinic function of EMAP II and its neutralization were assessed by migration in vitro and in vivo. We determined the location of EMAP II by immunohistochemistry, pulmonary proinflammatory and chemotactic gene expression by quantitative polymerase chain reaction and immunoblotting, lung outcome by pulmonary function testing and histological analysis, and right ventricular hypertrophy by Fulton's Index. In BPD, EMAP II initially is a bronchial club-cell-specific protein-derived factor that later is expressed in galectin-3

Indexed as

bronchopulmonary dysplasiaendothelial monocyte-activating polypeptide IIinflammationlung

Identifiers

PMID27254784
PMCPMC5070113
OpenAlexW2413354264

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.